ABSTRACT
Objective@#Neonatal exposure to propofol has been reported to cause neurotoxicity and neurocognitive decline in adulthood; however, the underlying mechanism has not been established.@*Methods@#SD rats were exposed to propofol on postnatal day 7 (PND-7). Double-immunofluorescence staining was used to assess neurogenesis in the hippocampal dentate gyrus (DG). The expression of p-Akt and p27 were measured by western blotting. The Morris water maze, novel object recognition test, and object location test were used to evaluate neurocognitive function 2-month-old rats.@*Results@#Phosphorylation of Akt was inhibited, while p27 expression was enhanced after neonatal exposure to propofol. Propofol also inhibited proliferation of neural stem cells (NSCs) and decreased differentiation to neurons and astroglia. Moreover, the neurocognitive function in 2-month-old rats was weakened. Of significance, intra-hippocampal injection of the Akt activator, SC79, attenuated the inhibition of p-AKT and increase of p27 expression. SC79 also rescued the propofol-induced inhibition of NSC proliferation and differentiation. The propofol-induced neurocognition deficit was also partially reversed by SC79.@*Conclusion@#Taken together, these results suggest that neurogenesis is hindered by neonatal propofol exposure. Specifically, neonatal propofol exposure was shown to suppress the proliferation and differentiation of NSCs by inhibiting Akt/p27 signaling pathway.
Subject(s)
Animals , Rats , Cell Proliferation , Hippocampus/metabolism , Neural Stem Cells , Propofol/toxicity , Proto-Oncogene Proteins c-akt/metabolism , Rats, Sprague-Dawley , Signal TransductionABSTRACT
Thorough excavation and artful utilization of various kinds concrete and invisible learning resources contribute to the cultivation of excellent postgraduates.In postgraduate education of anesthesiology Xuzhou Medical College utilizes time,network,technique platform,research outcome,self-potentiality and clinical patients resources,which produces an active effect and has important instructional significance.
ABSTRACT
<p><b>AIM</b>To study the effect of montelukast on apoptosis and Fas mRNA expression of eosinophils in airway of asthmatic guinea pigs.</p><p><b>METHODS</b>Experimental asthma model of guinea pigs was induced by ovalbumin. The eosinophils in broncho-alveolar lavage fluid (BALF) were separated by density gradient centrifugation. The apoptosis of eosinophils was labeled by TdT-mediated dUTP nick end labeling (TUNEL) technique. Fas mRNA expression of eosinophils was detected by reverse transcription-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>After treatment with montelukast, the number of eosinophils in BALF of asthmatic guinea pigs decreased significantly. The apoptosis index as well as Fas mRNA expression of eosinophils were elevated significantly. There were statistical differences between the therapeutic group and the model group.</p><p><b>CONCLUSION</b>Apoptosis of eosinophils is highly correlated with the increased expression of Fas mRNA. Enhancing expression of Fas mRNA and promoting apoptosis of eosinophils subsequentely may be an important mechanism for montelukast to antagonize airway inflammation of asthma.</p>